Extensive evidence supports the involvement cholecystokinin (CCK) in the peripheral and central nervous system control of food intake. A currently prevailing hypothesis suggests that CCK serves as the neurotransmitter in a polysynaptic ascending projection from the peripheral branches of the vague nerve to the hypothalamus and that these projections mediate short-term satiety. The proposed research is aimed at (1) localizing CCK-containing projections from vagal afferents to two hypothalamic nuclei and (2) determining the function of these projections in short-term satiety. These aims will accomplished through both anatomical and behavioral methods of inquiry. A combination of pathway tracing techniques and immunohistochemistry will be utilized to trace CCK-containing projections from vagal afferents terminating in the nucleus tractus solitarius to either the ventromedial or the paraventricular hypothalamic nuclei, including a possible relay in the parabrachial nucleus. The involvement of these projections in the control of food intake will be determined by assessing the effect on short-term food intake of direct injections of CCK receptor agonists and antagonists to the CCK terminal field areas and by determining the effect on meal patterning of physically disrupting a CCK projection. The information provided by these studies will be relevant to the treatment of eating disorders, particularly bulimia nervosa.